Mechanism that causes cancer to metastasize identified

Madrid, June 2 (IANS/EFE) An international team of researchers has found the mechanism whereby cancerous cells manage to spread from their original location to other parts of the body through the process known as metastasis.

The results of the study, headed by Manel Esteller, the director of the Cancer Epigenetics and Biology Program at the Bellvitge Biomedical Research Institute in Barcelona, Spain, will be published in the Nature Medicine magazine.

The study was conducted on melanomas — a malignant tumour associated with skin cancer, but the researchers found that this mechanism is also found in colon and breast cancer.

Metastasis is responsible for 90 percent of cancer deaths and understanding the mechanisms responsible for this process is one of the prime objectives of the research, Esteller said.

One of the tumours with the greatest ability to metastasize is melanoma, the incidence of which has increased in recent decades due to greater exposure to the sun.

The researchers, a group that also includes scientists with La Fe Hospital and the General Hospital of Valencia, compared the genetic material in the primary tumour’s cells with the genetic material from metastasized cells in the same patient.

Looking for differences, the researchers found that among all a patient’s genes, there is just one that clearly differs between those two groups.

That gene, known as TBC1D16, in the initial tumour is inactive or dormant, while in the metastasized phase it is active.

“This gene turns on like a light-bulb to guide metastasis and cause (those cells) to escape from their birth site,” Esteller said.

Specifically, what this gene does is to activate two more potent oncogenes, BRAF and EGFR, thus stimulating metastasis.

There is already a drug on the market that acts against these oncogenes and another is currently in clinical trials.

Esteller said that the next step is to convince pharmaceutical companies to include the TBC1D16 marker in their clinical trials.

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